Subject(s)
Apolipoprotein A-I/drug effects , Erythropoietin/therapeutic use , Kidney Failure, Chronic/blood , Peritoneal Dialysis , Adult , Aged , Anemia/drug therapy , Anemia/etiology , Apolipoprotein A-I/blood , Diabetes Mellitus/blood , Erythropoietin/pharmacology , Female , Humans , Kidney Failure, Chronic/therapy , Male , Peritoneal Dialysis/adverse effects , Retrospective StudiesABSTRACT
Reference values are presented for the activity of fructose-1-phosphate aldolase (F1PA) and fructose-1,6-bisphosphate aldolase (FBPA) in the small intestinal mucosa of 32 nonaffected children, 8 nonaffected adults and 2 children with hereditary fructose intolerance (HFI). The 96% confidence limits for F1PA in children are 1.55 to 43.0 u/g protein, completely distinct from the results of the two affected children (1.3 and less than 0.1 u/g protein). With fructose-1,6-bisphosphate as subtrate, the 96% confidence limits are 10 to 324 u/g protein and the values for the two affected children, 23.7 and 9.3 u/g. Among the nonaffected children two mucosal biopsies with F1PA activities less than 1.55 u/g were found. In one mucosal biopsy among the nonaffected children an FBPA activity less than 10 u/g was recorded. The data are interpreted as indicating that the determination of F1PA activity in intestinal mucosa is a highly sensitive test in detecting individuals with HFI. However, the specifity of the test is not absolute. Diagnosis should be based on both clinical and laboratory considerations. The determination of FBPA activity in the same biopsy specimen does not contribute substantially to the differential diagnosis.
Subject(s)
Duodenum/enzymology , Fructose-Bisphosphate Aldolase/metabolism , Intestinal Mucosa/enzymology , Adult , Child , Fructose Intolerance/diagnosis , Fructose Intolerance/enzymology , Fructose Intolerance/genetics , HumansABSTRACT
Lactating white rats (Rattus norvegicus) were subjected to metabolic and respiratory acidosis and metabolic alkalosis. Before and during the various treatments, the acid-base status of heart blood and milk was determined. Acute metabolic acidosis lowered the pH of plasma and milk; Pco(2) and bicarbonate concentrations in plasma were lowered, and in milk Pco(2) was raised and the bicarbonate concentration remained unchanged. Respiratory acidosis and acetazolamide caused a drop in blood pH and in blood and milk bicarbonate concentrations; milk pH remained unchanged, but Pco(2) was raised in both plasma and milk. Acute metabolic alkalosis raised the blood pH and milk Pco(2); plasma Pco(2) and bicarbonate concentrations in blood and milk remained unchanged. The data show that greater changes occur in acid-base parameters of blood than milk when animals are exposed to acidifying and alkalinizing stimuli.
